Poly(ADP-ribose) polymerase-1 promotes expression of miR-155 by the up-regulation of methyl-CpG binding domain protein 2 in TK6 cells exposed to hydroquinone
Autor: | Linhua Liu, Junli Shao, Xiaoxuan Ling, Baisen Zhong, Minhua Wu, Haiqiao Zhang, Zhiming Gui, Jianming Peng, Zhijie Pan, Jieyou Li, Qian Yuan, Qiang Tan, Zhidong Liu |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
DNA damage Poly ADP ribose polymerase Poly (ADP-Ribose) Polymerase-1 Toxicology Cell Line Histones 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Gene expression MG132 medicine Humans Gene knockdown Chemistry Activator (genetics) Lymphoblast Acetylation General Medicine Molecular biology Hydroquinones Up-Regulation DNA-Binding Proteins MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Proteasome inhibitor medicine.drug |
Zdroj: | Toxicology in Vitro. 55:51-57 |
ISSN: | 0887-2333 |
Popis: | Hydroquinone (HQ), one of the major metabolites of benzene, can induce aberrant gene expression. MiR-155, a tumor activator, participates in various biological processes, including DNA damage response. However, the molecular mechanism of aberrant miR-155 expression is still not completely elucidated. Here, we investigated the mechanism of abnormal expression of miR-155 induced by poly(ADP-ribose)polymerase-1 (PARP-1) expression in HQ-treated TK6 lymphoblastoid cells. We examined the expression of genes related to abnormal expression of miR-155 to explore the reason for this phenomenon. The results of the present study showed that miR-155 was significantly increased and reactive oxygen species (ROS) were decreased in cells treated with HQ for 72 h compared with PBS-treated cells. Meanwhile, E4F1, PARP-1 and PARP-1 related co-regulators (NF-κB, HDAC1, and HDAC2), acetylated histone H3 (H3Ac) were increased in a concentration-dependent manner. Experiments for treatment with 5-AzaC (DNMTs inhibitor), TSA (HDACs inhibitor), DOX (to activate PARP-1) or MG132 (proteasome inhibitor) revealed that the MBDs and PARP-1 was positively associated with miR-155 expression. Moreover, in cells treated with HQ in conjunction with PARP-1 knockdown, expression of miR-155, H3Ac and MBD2 protein were decreased, compared with negative control. In conclusion, PARP-1 activates expression of miR-155 via acetylation by regulating MBD2 in TK6 cells exposed to HQ. |
Databáze: | OpenAIRE |
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